Narrative review discusses MEMR and MOCR recording techniques in aging adults with and without hearing loss.

The middle ear muscle reflex (MEMR) and medial olivocochlear reflex (MOCR) are increasingly studied for their role in suprathreshold auditory processing. However, recording these reflexes in humans is potentially complicated by age-related (sub)clinical hearing loss and co-activation. This study investigates (1) the influence of age-related (sub)clinical hearing loss, (2) methodological differences between conventional and wideband MEMR techniques, and (3) how MEMR activation contaminates MOCR recordings. Three test groups were included: young normal-hearing adults, middle-aged normal-hearing adults, and middle-aged adults with audiometric hearing loss. Cochlear status and neural encoding was assessed using distortion-product otoacoustic emissions (DPOAEs) and envelope following responses (EFRs). MEMR recordings were compared using conventional tonal stimuli and wideband stimuli. MOCR was recorded at elicitor levels of 60 and 75 dB to evaluate MEMR co-activation. MEMR was related to age, suggesting sensitivity to subclinical cochlear damage. Wideband stimuli were beneficial as elicitor (noise vs. tone), while changing the probe stimuli added no significant benefit (click vs. tone). MOCR strength did not correlate with age-related subclinical hearing, suggesting that MOCR measurements may reflect efferent function relatively independently of afferent sensorineural status in audiometric normal hearing subjects. However, reliable recordings were challenging in participants with audiometric hearing loss due to poor OAE baselines. MEMR co-activation was detectable in the click response and could alter MOCR-induced suppression. These findings suggest that, in cases of normal hearing thresholds, MEMR amplitude may be a marker of subclinical cochlear damage and MOCR measurements may more specifically reflect efferent function. Clinical measurements can be improved using broadband stimuli, accounting for outer-hair-cell damage, and defining criteria for reflex co-activation.